多巴胺之促成EDTA抑制黑質緻密部細胞之活動

Abstract

250-350克的雌性大白鼠經Urethane麻醉後，固定在腦立體定位儀上，利用玻璃微電極記錄黑質緻密部多巴胺細胞的自發性放電。並觀察皮下注射EDTA對黑質多巴胺細胞之影響，及合成類嗎啡Fentanyl和多巴胺拮抗劑對此影響有何效應。當給予大白鼠EDTA時，大部分的黑質多巴胺細胞都受到明顯的抑制，平均抑制50.8 ±2.6%；而這種抑制大都(89.3%以上)因靜脈注射Fentanyl (2μg/kg), Haloperidol (0.125mg/kg)和Chloropromazine (1mg/kg)而被抵消。Fentanyl抵消EDTA所造成之抑制又因靜脈注射Naloxone (0.2mg/kg)而完全被對抗。Haloperidol和Chloropromazine是多巴胺的拮抗劑，因此可推論黑質多巴胺細胞活動之抑制可能是EDTA引起疼痛刺激所造成，而且是由多巴胺所促成的。After the urehane anesthetized rats were mounted in the stereotaxic instrumernt, the effects of ethylenediamine tetraacetic acid (EDTA) on the neuronal activity of the substantia nigra pars compacta (SNC) neurons were studied. The neuronal activity was recorded extracellularly with glass micropipette electrodes. Following intradermal injection of EDTA (2.5%, 0. 05ml) at the hind paw, the firing rates of SNC neurous were decreased, i.e. the neuronal activity of SNC neurons was inhibited by EDTA. The inhibition of SNC neurons by EDTA was cancelled by the intravenous injection of Fentanyl (2.5 μg/kg) then the Fentanyl cancellation of the inhibition of SNC neurons by EDTA was antagonized by Naloxone (0.2mg/kg i.v.), thus, it can be suggested that the stimulus induced by EDTA is painful in nature. Furthermore, the inhibition of SNC neurons by EDTA could be antagonized by Haloperidal (0.125mg/ kg, i.v.) and Chlorpromazine (1mg/kg. i.v.) which are dopamine receptor blockades, therefore, it can be indicated that the inhibition of SNC neurons by EDTA is mediated by dopamine.